Hao et al reported that DUSP1 increased the phosphorylation of p53 at the S15, S20, and S46 sites in HCC cells by inhibiting p38 MAPK phosphorylation, while the enhanced p53 activation induced the expression of the target genes p21 and p27, suggesting that DUSP1 and p53 may suppress HCC occurrence and development through the cooperation of active regulatory circuits.26Lopez-Yus et al reported that the expression of DUSP1 paralleled the degree of steatosis, and DUSP1 could be a key player in the progression of NAFLD.27 This evidence concerns the gene DUSP1 and steatosis.